The sensitivity and specificity of such findings are limited. With respect to “muscle enzymes”,

only the measurement of serum creatine kinase (sCK) activity is indicated in clinical practice. There is no longer any value in measuring other enzymes, such as aldolase. It must be remembered that AST and ALT are muscle as well as liver enzymes–that they are measured so frequently in routine clinical practice means that their increase may be the first pointer to a muscle disease, Metformin in vivo but they have no advantage over sCK. sCK is often increased in the inflammatory myopathies, and monitoring its fall in response to treatment is undoubtedly helpful. But it is not invariably raised in active disease, either before treatment is initiated, or during relapse when on treatment. In summary, the nearest that we have to any form of gold standard is the immunopathological study of muscle. However, even that has limitations. To

demand the demonstration of such changes may hamper both routine clinical practice and research. Specific changes may be absent simply due to the vagaries of sampling. The same pathological changes may be seen in very different clinical settings. Useful classification systems thus depend upon a combination of clinical, pathological and other laboratory features. As with many areas of myology, historical description of myositis dates back two centuries, but what can be considered the modern era started only in the 1950s–a period when clinicians first made rigorous attempts to classify the different forms of muscle disease and new muscle biopsy staining techniques were being developed. Eaton reported on 41 cases, only including clinical, neurophysiological Src inhibitor and pathological findings [5]. His cases included many with DM or scleroderma. Walton and Adams published a monograph (“Polymyositis”) in which

they reviewed the literature and reported detailed clinical and laboratory findings in 40 patients [6]. As was to be the case for another 30 years they considered DM and PM to be essentially the same, differentiated only by the presence or absence of a rash. Even without a rash they noted that PM could be acute, but also that chronic PM was difficult to distinguish clinically and sometimes pathologically from the dystrophies. The relationship with neoplasia was “sufficiently clear to indicate that a careful search should be made for malignancy in any patient suffering from DM or PM”. They also noted the close relationship with collagen disease–“Sometimes the symptoms and signs of muscle disease are predominant, but in other cases they are obscured by skin changes or the manifestations of an associated collagen disease. Even when the muscle weakness is predominant there may be features such as the Raynaud phenomenon, localised scleroderma of the hands or rheumatoid arthritis…”. Their clinical classification is given in Box 1. As will be seen, it is remarkable how similar this looks to all future attempts at reclassification. 1.

One possible explanation is that over-expansion of the thorax and lungs allows for increased alveolar flooding in excess of base line aeration resulting in approximately unaltered ALVs between the two groups. Another explanation is that the inflamed and oedematous areas were aerated less than normal, but because the unaffected see more areas of lung were aerated more than normal (hyperinflation

or emphysema), the overall ALV values remained approximately unaltered. Nevertheless, these ALV profiles provide more detailed knowledge about the influenza-induced respiratory disease development than confined data obtained from a single predefined read out. Moreover, survival and recovery from challenge infection can be included in this set-up and with the opportunity to still measure the development of serum antibody responses

upon challenge infection. Upon necropsy, the relative lung weights (RLWs) of the intranasally immunised ferrets was about 2-fold lower (Mann–Whitney, two-tailed, P < 0.0047) as compared to those of the placebo-treated animals ( Fig. 3), which is in agreement with the absence of pulmonary ground-glass opacities. Usually, more severely affected and inflamed lungs with increased amounts of fluid are heavier compared to normal or less affected lungs. This Palbociclib price translates within the ferret model in influenza research to RLWs ≤ 1.0 associated with non- to minimally affected lungs and RLWs > 1.0 associated with Fossariinae severe pulmonary inflammation with oedema [12], [19] and [20]. In conclusion, the implementation of consecutive CT imaging enables repeated in vivo measurements of lung aeration as parameter to evaluate vaccine efficacy in preclinical protocols. Consecutive day to day imaging overcomes the limitations entailed by necropsy at a predefined time point after infection, and the lung capacity can be repeatedly quantified in real-time. We are grateful to Willem van Aert, Ronald Boom, Cindy van Hagen, Rob van Lavieren from ViroClinics Biosciences B.V., Peter van Run from the Department of Virology Erasmus MC Rotterdam,

and Dennis de Meulder from the Erasmus Laboratory Animal Science Center Rotterdam for their excellent technical assistance and analyses. Conflict of interest: The authors EVK, VT, KS, GvA, LdW, and AO are affiliated with Erasmus MC spin-off company ViroClinics BioSciences B.V. The author JH is affiliated with Karolinska Institutet spin-off company Eurocine Vaccines AB. “
“Despite progressive increases in seasonal influenza vaccine coverage, influenza-related morbidity, mortality, and hospitalization rates remain high and have continued to increase in older adults (≥65 years of age) [1]. Up to 90% of all annual influenza-related deaths occur in the older adults [2], whose aging immune systems respond weakly to vaccines and are less able to combat infection [1], [3], [4] and [5].

Moreover, the capacity to continue cell growth at the moment of virus infection may be important as the applied MOI was 0.01 which means 99% of the cells will not be infected during the first virus replication cycle and can potentially grow further. These topics are currently under investigation to be able to further optimize the virus culture at increased cell densities. The highest virus yields, based on d-antigen concentrations, were observed using the recirculation mode for cell culture. At the first glance, to maximize bioreactor capacity, this seems to be the best choice. However, it should be Pictilisib solubility dmso mentioned that a larger pre-culture needs to be prepared

as here the cell culture is started at 0.6 × 106 instead of 0.1 × 106 cells mL−1 used for the other cell culture strategies. Hence, extending the overall process throughput time. Further, considering the cell specific d-antigen productivity, the semi-batch cell culture strategy appeared to be a good alternative. In addition, this method can be applied in existing manufacturing equipment without large

investments. At present, we are optimizing this method with respect to microcarrier concentration, feed frequency and feed/bioreactor volume Lumacaftor clinical trial ratio. In addition, adaptation of downstream processing to concentrate and purify the poliovirus obtained from increased cell density cultures is studied. Focus points are the filter load with cell debris during clarification and concentration and the removal of the increased concentrations of host cell proteins and host cell DNA during column chromatography. Also, product quality and immunogenicity after purification remains to be assessed. In that way, discrimination between intact virus particles and virus progeny, which may have attributed to the observed increased d-antigen levels, can be made. This study shows that adherent Vero cell culture using different methods of medium refreshment allows higher cell densities. Increased cell densities allowed up to 3 times higher d-antigen levels when compared with that

obtained from batch-wise Vero cell culture. The cell specific d-antigen production was lower when cells were medroxyprogesterone infected at higher cell densities. Application of a semi-batch mode of operations allowed the highest cell specific d-antigen production, while 2 fold lower cell specific d-antigen yields were found using perfusion or recirculation cultures. This reduction may be related to the presence of multilayers of cells on the microcarriers, which were observed at higher cell densities that were reached using perfusion or recirculation mode. In our view, the most promising concept for polio d-antigen yield optimization would be semi-batch cultivations. This strategy has potential to be further improved and can be implemented in current manufacturing facilities. Using the here presented method for semi-batch cell culture and subsequent virus culture, d-antigen yields per run can be doubled.

The physical form of prednisolone within the 3D printed tablets was investigated using thermal and diffractometry methods. Thermal analysis (DSC) showed prednisolone crystals to have a peak at 203 °C corresponding to the melting point of prednisolone (Fig. 5). The prednisolone loaded tablet showed a glass transition temperature (Tg) of 45 °C whereas PVA filament appeared Selleck EGFR inhibitor to have a Tg of 35 °C. It was expected that the Tg of prednisolone loaded tablet to be lower than PVA filament due to the plasticizing effect of prednisolone. Such an increase in the Tg could be attributed to loss of plasticizer(s) in the PVA during incubation in methanol for drug loading.

The absence of such an endothermic peak of prednisolone in drug loaded tablets suggested that the majority of prednisolone is in amorphous form within the PVA matrix. On the other hand, XRPD indicated typical peaks of prednisolone at 2Theta = 8.7, 14.7 and 18.6 (Fig. 6) (Nishiwaki et al., 2009). The absence of such peaks in prednisolone loaded tablets suggested that the majority of prednisolone exists in amorphous form. Both blank PVA filament and drug loaded PVA tablets showed peaks at 2Theta = 9.3°, 18.7° and 28.5°. Such peaks may be related to the semi-crystalline structure of PVA (Gupta et al., 2011). As the exact PVA filament composition was not disclosed by the manufacturer, it was selleck compound not

possible to attribute these peaks. In vitro release pattern of prednisolone from 3D printed PVA tablets was studied via a pH-change flow-through cell dissolution system. Fig. 7 indicated that prednisolone tablets with different weights exhibited a similar in vitro release profile. The majority of drug release (>80%) took place after 12 h for 2 and 3 mg tablets and over 18 h for tablets with doses of 4, 5, 7.5 and 10 mg.

Approximately 100% of prednisolone release was attained within 16 h for tablets with 2 and 3 mg drug loading. isothipendyl The faster release of prednisolone from the smaller size tablets is likely to be related to their larger surface area/mass ratio which promotes both drug diffusion and the erosion of PVA matrix. By the end of the dissolution test (24 h), it was visually evident that the tablet had completely eroded within the flow-through cell. Several studies reported PVA to form a hydrogel system where drug release is governed by an erosion mechanism ( Vaddiraju et al., 2012 and Westedt et al., 2006). In summary we have reported a significant adaptation of a bench top FDM 3D printer for pharmaceutical applications. The resultant tablets were solid structures with a regular ellipse shape and adjustable weight/dose through software control of the design’s volume. This fabrication method is applicable to other solid and semisolid dosage forms such as implants and dermal patches. FDM based 3D printing was adapted to engineer and control the dose of extended release tablets.

Qc: Rf = 0.66, MP = 168 °C–173 °C, λmax (UV) = 252.8 nm, IR (KBr) cm−1: 3326 cm−1 (NH stretching), 3120 (CH stretching), 1701 cm−1 (carbonyl group C O), 1660 cm−1, 1585 cm−1 (C C stretching), 777 cm−1 (para substituted benzene) 840 cm−1, 742 cm−1 (aromatic region). 1H NMR (400 MHz, DMSO) δ (ppm): 8.75 (s, 1H), 8.59 (s, 1H), 8.04 (d, J = 8.4 Hz, 1H), 7.93 (d, J = 8.4 Hz, 1H), 7.86–7.80 (m, 1H), 7.66 (d, J = 8 Hz, Trichostatin A solubility dmso 2H), 7.43, 7.40 (m, 1H), 7.26 (d, J = 8.4 Hz, 1H), 6.59 (s, 1H), 6.59 (d, J = 8.4 Hz, 2H). Qd: Rf = 0.62, MP = 218 °C–220 °C, λmax (UV)

– 252.8 nm, IR (KBr) cm−1: 3121 cm−1 (NH stretching), 2920 cm−1 (CH Wnt activity stretching), 1700 cm−1 (carbonyl group C O), 1582 cm−1 (C C stretching), 776 cm−1 (para substituted benzene) 841 cm−1, 745 cm−1 (aromatic region). 1H NMR (400 MHz, DMSO) δ (ppm): 12.56 (s, 1H), 9.34 (s, 1H), 8.79 (s, 1H), 8.75 (d, J = 2 Hz, 1H), 8.04 (d, J = 8.4 Hz, 1H), 7.94 (d, J = 8.4 Hz, 1H), 7.66 (d, J = 8.4 Hz, 2H), 7.25 (dd, 1H, J = 2.4 Hz, 8.8 Hz, 1H), 7.42 (s, 1H), 7.36 (s until 1H). Qe: Rf = 0.69, MP = 214 °C–216 °C, λmax (UV) = 255.2 nm, IR (KBr) cm−1: 3127 cm−1 (NH stretching), 2917 cm−1 (CH stretching), 1632 cm−1 (carbonyl group C O), 1586 cm−1 (C C stretching), 782 cm−1 (para substituted benzene), 843 cm−1, 748 cm−1, (aromatic region). 1H NMR (400 MHz, DMSO) δ (ppm): 9.04, 8.57 (s, 1H), 8.76 (s, 1H), 8.05 (d, J = 8.8 Hz, 1H), 7.81–7.77 (m, 1H), 7.95 (d, J = 7.6 Hz, 2H),

7.68 (d, J = 8 Hz, 2H), 7.48–7.46 (m, 1H), 7.40–7.37 (m, 1H), 7.31 (d, J = 8.4 Hz, 1H), 7.27 (d, J = 8.8 Hz, 1H). Qf: Rf = 0.64, MP = 208 °C–210 °C, λmax (UV) – 245.6 nm, IR (KBr) cm−1: 3124 cm−1 (NH stretching), 2970 cm−1 (CH stretching), 1700 cm−1 (carbonyl group C O), 1603 cm−1, 1590 cm−1 (C C stretching), 776 cm−1 (para substituted benzene), 842 cm−1, 746 cm−1, (aromatic region). 1H NMR (400 MHz, DMSO) δ (ppm): 12.67 (s, 1H), 8.86 (s, 1H), 8.76 (s, 1H), 8.06 (d, J = 8.4 Hz, 2H), 7.47–7.44 (m, 2H), 7.14–7.08 (m, 2H), 7.97 (d, J = 8.4 Hz, 1H), 7.67 (d, J = 8.4 Hz, 1H), 7.26 (d, J = 8.4 Hz, 2H). QN-D: Rf = 0.63, MP: 178 °C–180 °C, λmax (UV) – 267 nm, IR (KBr) cm−1: 3454 cm−1 (NH stretching), 3365 (CONH), 3053 (Ar Ch stretching), 1685 cm−1 (carbonyl group C O), 1691 cm−1 (C C stretching), 825 cm−1 (para substituted benzene), 761 cm−1 (para chloro).

The collected samples were stored at 4 °C. Starch degrading microbes were isolated using Strach Agar Medium (SAM). The isolates showing maximum clear halo zone were sub-cultured.7 Selective isolates with maximum starch degrading activities were identified up to species level.8 and 9 The most potent isolates were finally chosen for further studies. The inoculum for further enzyme modulation and other studies was prepared using Luria

Broth (LB) medium. The fresh overnight culture was used as an inoculum for the production of amylase.10 The inoculated medium was incubated at 37 °C for 48 h by shake flask fermentation method at 200 rpm. The culture broth was then centrifuge at 8000 × g 10 min at 4 °C. The free cell supernatant Galunisertib price was used as an extracellular crude enzyme. 11 Total protein concentrations were determined by Bradford’s method using Bovine Serum Albumin (BSA) as the protein standard.12 α-Amylase activity was determined by measuring the formation of reducing sugars released during starch hydrolysis. The amount of liberated reducing sugar was determined by Dinitrosalicylic acid (DNS) method. Glucose was used to construct www.selleckchem.com/products/Dasatinib.html the standard curve.4 Five percent bacterial inoculum was added aseptically to 500 ml of sterile growth

medium and incubated at 37 °C at 150 rpm. Twenty ml of culture was taken periodically for 48 h at every 6 h intervals. The amylase activity was determined in the culture filtrate. The effect of pH on amylase activity was determined at different pH (6.5, 7, 7.5, 8, 8.5 and 9) and the effect of temperature on enzyme activity was determined using different temperature (26 °C, 29 °C, 32 °C, 35 °C, 38 °C and 41 °C).11

Different carbon and nitrogen sources (both at concentration of 10 g/L) were used in minimal medium, pH 7 and incubated at 32 °C for 24 h. Similarly different amino acids like glycine, alanine, aspartic acid and cysteine were used in the medium for optimization.13 The culture filtrates were assayed for total protein content below and amylase activity. The culture filtrate was precipitated using 80% w/v Ammonium sulfate precipitation method.14 Then the precipitate was separated by centrifugation at around 6700 × g for 10 min. The pretreatment of the dialysis membrane was done Ashwini et al, 2011. Genomic DNA was extracted using phenol–chloroform extraction method. The PCR parameters for the amplification of 16S ribosomal DNA were optimized. 50 μl of PCR master mix contained universal primer set 27 F- (5′-AG AGT TTG ATC MTG GCT CAG-3′)/1492 R- (5′-G GYT ACC TTG TTA CGA CTT-3′), 10 mM dNTPS, 10× PCR Buffer, 1 U Taq DNA polymerase, 2 mM Mg+ and (100–200 ng) template DNA. PCR steps included initial denaturation at 95 °C for 5 min, 35 cycles of denaturation at 95 °C for 1 min, annealing at 56 °C for 2 min, elongation at 72 °C for 1 min and final extension at 72 °C for 10 min. Approximately 1.5 kb amplicons were generated.

6). In addition, once vaccine coverage levels exceed Cobimetinib molecular weight 75%, the model predicts biennial patterns in rotavirus activity. This activity becomes increasingly more irregular and infrequent as coverage levels approach 100%. Whether vaccination immunizes only against a primary infection

or each dose immunizes against a corresponding natural infection, minimal differences in impact are seen between two or three dose vaccine schedules (Fig. 6). We found that our original model provided the best fit to the real data (Table 3). When duration of infectiousness, risk of becoming re-susceptible after each infection and proportion symptomatic at each infection were set at values greater than the original estimates, the predicted reduction in rotavirus

cases observed after the introduction of vaccination was less dramatic (Table 3). This is an important observation. In developing countries, child malnutrition may result in more symptomatic infections and poorer access to treatment may prolong the duration of infectiousness. This could result in the vaccine being less effective in reducing disease burden in these settings. We found that rotavirus disease patterns in England and Wales can be modelled well by a dynamic model of rotavirus transmission which takes into account the natural history of rotavirus infections. The model reproduces the regular seasonal pattern of rotavirus gastroenteritis and the age distribution of cases seen. Vaccination is expected to reduce the observed seasonal peak in rotavirus Nutlin-3a mouse disease incidence and reduce the overall burden of disease. Model fit was obtained by using a cosine function for the seasonal variation in transmission. Understanding the driving forces underlying this seasonality remain elusive because it

is difficult to prove that common seasonal patterns between environmental exposures and disease incidence are not the result of some other underlying factor. However, low relative humidity and low temperature may explain short-term variations in rotavirus disease incidence [34] and [35]. Therefore it is plausible, that in part, these weather factors are responsible for seasonal patterns of rotavirus disease. Pitzer et al. [29] have developed a seasonally forced age-stratified transmission model for rotavirus which predicts rates unless of rotavirus hospitalisations in the United States similar to those observed. The model differs to our model in a number of ways. Some of the differences in model assumptions may be due to the different types of data used in model fitting: Pitzer et al. fitted their model to hospitalization data for children <5 years, while in this study we fitted our model to laboratory surveillance reports for all age groups. Firstly, we included up to three potentially symptomatic re-infections, based on careful follow-up studies [15] and [18], whereas Pitzer et al.

The drug standard was exposed to 0.1 N HCl solution, 0.1 N NaOH and 1% peroxide solutions for 24 h at room temperature. To study the percent of degradation in the presence

of light and thermal conditions the standard was exposed to UV light and a temperature of 45 °C separately for about 36 h. In each case a working standard (10 μg/mL) solution was prepared, injected into Autophagy Compound Library the system and the chromatograms were recorded. The amount of drug degraded was calculated by comparing the area of the standard with that of the area of the degraded sample. The results are presented in Table 4 Comparisons of results of proposed method with reference method were presented in Table 5. The components were separated under a simple isocratic mode in the developed method where as gradient elution mode was used in the reference method. The retention time and run time of the proposed method and reference method were found to be 0.595 min & 3.0 min and 1.174 min & 4.0 min, therefore the developed method was found to be fast and economic. The LOD and LOQ values of developed method were very less than the values www.selleckchem.com/products/jq1.html reported in the reference method therefore the proposed was more sensitive

than the reported method. The proposed method was found to be simple, fast, precise, accurate, rugged and economic. The drug was found to be stable under the different stressed conditions. Therefore the developed method can be used as an alternative method for routine analysis in quality control. All authors have none to declare. The authors would like to thank to Dr. Reddy’s Laboratory for gifted samples

and Pharma Train, an analytical testing laboratory Hyderabad for providing laboratory facilities, and to the authorities of Acharya Nagarjuna University for providing heptaminol provision for research work. “
“Ricinus communis Linn. (Erandi) belongs to family Euphorbiaceae is a monotypic genus. It is found throughout the country and widely cultivated in the tropics and warm regions for its seeds, which yield the well known castor oil. The castor is one of the major oil seed crops of India and, in fact India is the second largest producer of castor seed in the world. Ricinus communis Linn. is believed to be a native of tropical Africa. The world production is about 1,10,000 tonnes/annum observed by Kirtikar and Basu, 1935. 1 The plant contains alkaloids, ricinoleic acid, stearic, linoleic, palmitic acid, sitosterol, squalene (38 mg/100 g) tocopherols and stearic acid (Chatterjee, and Prakashi, 1994 2). Plants also have toxic constituents like ricinine and ricin. The root of Ricinus is sweet in taste and used as medicine. Leaves are useful in intestinal worms, strangury, night blindness, etc. The flowers are also useful in glandular tumours & anal troubles. The fruit is useful in piles. The seed is cathartic and aphrodisiac.

An approximation of lifetime cost was obtained by multiplying the average annual cost by the estimated average survival time for patients with incident CC in each country over the 5 years post diagnosis. It was assumed that a cancer patient

alive for 5 years post diagnosis is cured and hence without any treatment and costs associated. The average survival time was estimated for each country using data on the number of annual incident cases and estimates learn more of 5 year prevalence reported by Globocan 2008 [1] as follows: (5⁡ years prevalent cases/incident cases×5)×5=average survival over the 5 years post diagnosis(5⁡ years prevalent cases/incident cases×5)×5=average survival over the 5 years post diagnosis Costs for CC treatment were expressed in local currency and updated to 2011 values using the country-specific Consumer Price Index reported by the World Bank for each country [20]. Estimated survival times and lifetime costs are shown in Table 1. The potential annual effect of HPV vaccination on the burden related to CIN 2/3 at vaccination steady state was estimated in two countries: Italy and Malaysia, randomly selected based on data availability. The method used is identical to the one used to estimate the vaccine impact

on CC cases and deaths. The number of CIN2/3 cases prevented with vaccination irrespective of HPV type, the expected number of HPV-16/18 related CIN2/3 avoided by vaccination cases as well as the difference between the two were estimated. selleck chemicals Vaccination coverage was assumed to be 80% in both countries. The prevalent annual numbers of CIN2/3 lesions prior to the introduction of vaccination for Italy and Malaysia were retrieved from literature (Table 2) [5] and [21]. The vaccine effectiveness

Oxalosuccinic acid against CIN2/3 lesions irrespective of HPV type was assumed at 64.9% based on the VE reported against CIN2+ lesions, irrespective of HPV type in the HPV-naïve1 TVC from the end-of-study results from the PATRICIA trial [9]. Vaccine effectiveness against CIN2/3 lesions related to HPV-16/18 was estimated based on the effectiveness against HPV-16/18 CIN2/3 lesion and the proportion of CIN2/3 related to HPV-16/18. The vaccine effectiveness against HPV-16/18-related CIN2/3 lesions was assumed to be 100%, based on VE against CIN2+ causally related to HPV-16/18 reported from the end-of-study from the PATRICIA trial among the HPV-naïve1 TVC [9]. The proportion of CIN2/3 related to HPV type-16/18 was calculated based on the HPV-16/18 distribution reported for high-grade cervical lesions in the ICO HPV Information Centre database for each country [2] (Table 2). The expected CIN2/3-related treatment costs potentially offset by HPV vaccination was estimated assuming that 100% of CIN2/3 lesions prevented by vaccination would be treated. The offset on treatment costs was estimated by multiplying the number of cases potentially prevented by the CIN2/3 treatment unit cost.

The location of antibody binding sites (epitopes) or escape from binding can also be inferred from correlating the antibody cross-reactivity of viruses to their capsid sequence similarities [11]. Epitopes can also be predicted, in the absence of antibody recognition data, using different epitope

prediction programmes using viral crystal structure [12]. However, there are no reports for analysis of epitopes or vaccine strain selection studies using serotype A isolates originating from East Africa. Selleck Autophagy inhibitor Most FMD outbreaks in East Africa have been caused by serotype O, followed by serotype A and SAT-2 [13], [14] and [15]. The serotype A viruses are present in all areas of the world where FMD has been reported and are diverse both antigenically and genetically. More than 32 subtypes [16] and 26 genotypes of serotype A FMDV have been reported [17]. Control of FMD mainly depends on the availability Dabrafenib order of matching vaccines that can be selected based on three criteria: epidemiological information, phylogeny of the gene sequence for evolutionary

analysis and serological cross-reactivity of bovine post-vaccinal serum (bvs) with circulating viruses [18] and [19]. Mono-, bi- and quadri-valent vaccines are currently in use in East African countries for FMD control [20], [21] and [22]. These vaccines are mainly produced in vaccine production plants located in Ethiopia and Kenya using relatively historic viruses

and regular vaccine matching tests to select the best vaccine for use in the region are rarely carried out. Hence, the existing vaccines may not provide optimal protection against recently circulating FMD viruses. This study was, therefore, designed to characterise recently circulating FMD viruses in the region both antigenically and genetically and recommend matching vaccine strains SPTLC1 for use in FMD control program in East African countries. Fifty-six serotype A viruses from Africa submitted to the World Reference Laboratory for FMD (WRLFMD) at Pirbright were used in this study. These viruses were from five East African countries, Ethiopia (n = 8), Eritrea (n = 9), Sudan (n = 6), Kenya (n = 6), Tanzania (n = 7) and from three neighbouring countries: Democratic Republic of Congo (COD, n = 5), Egypt (n = 10) and Libya (n = 5). These samples are known to have been derived from cattle epithelial tissues except eight viruses from Egypt and one virus from Kenya where the host species is not known (Supplementary Table 1). All the samples were initially grown in primary bovine thyroid cells (BTY) with subsequent passage in either BHK-21 or IB-RS2 cells. The virus stocks were prepared by infecting cell monolayers and stored at −70 °C until use. Viruses are named according to a three letter code for the country of origin followed by the isolate number and the year of isolation, e.g. A-COD-02-2011.